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Abstract Background The association between fish consumption and risk of bladder cancer has not been established yet. The results from epidemiological studies are inconsistent. Methods We conducted a meta-analysis of cohort and case-control studies on the relationship between fish intake and bladder cancer. We quantified associations with bladder cancer using meta-analysis of relative risk associated to the highest versus the lowest category of fish intake using random effect models. Heterogeneity among studies was examined using Q and I2 statistics. Publication bias was assessed using the Begg's funnel plot. Results Five cohort and 9 case-control studies were eligible for inclusion. The combined relative risk showed that fish consumption was negatively, but not significantly, associated with a decreased risk of bladder cancer (relative risk, 0.86; 95% confidence interval, 0.61-1.12). In subgroup analyses, there was no evidence that study design, geographical region, case sample size, or exposure assessment substantially influenced the estimate of effects. Conclusion The overall current literature on fish consumption and the risk of bladder cancer suggested no association. Because of the limited number of studies, further well-designed prospective studies are needed to explore the effect of fish on bladder cancer.

Background and Objectives: Overconsumption of drinks containing fructose increases the risk for hyperuricemia and gout. Comparative analysis evaluating the indicators of serum uric acid (SUA) load caused by natural food-derived fructose and pure fructose in sweeteners is lacking. We aimed to uncover the effect of fructose from apple and honey and pure fructose powder on the SUA concentration of healthy young Chinese individuals.Methods and Study Design: Two randomized crossover trials were performed. The participants were randomly assigned to consume apple or honey (test food) or pure fructose powder (reference food); one week later, the groups' dietary intervention was switched. Blood samples were collected at 0, 30, 60, and 120 min after meal to measure the SUA and blood glucose concentrations.Results: At 30 and 60 min, the SUA concentration in participants consuming apple or honey was lower than in those consuming fructose powder. At 120 min, the SUA concentration of participants consuming apple returned to baseline. The areas under the curve (AUC) within 2 h (2h- AUCs) of SUA exhibited the trend of fructose >honey >apple. The 2h-AUC ratio between test food and reference food was determined using the uric acid index to assess the efficiency of food-derived fructose in increasing the SUA concentration. The uric acid index of honey was higher than that of apple. Men had higher postprandial SUA concentration than women.Conclusions: Food-derived fructose caused a lighter load on uric acid metabolism than pure fructose. Uric acid index can be useful for distinguishing fructose-containing foods. [ABSTRACT FROM AUTHOR]

Background: Clear cell renal cell carcinoma (ccRCC) is a common and aggressive renal cancer with high mortality when metastasized. Cancer-associated fibroblasts (CAFs) are pivotal in ccRCC evolution; however, their significance in forecasting prognosis and guiding therapy is undetermined., Method: We used Weighted Correlation Network Analysis to identify modules correlated with CAFs in bulk RNA-seq data. We also screened fibroblast marker genes in single-cell RNA-seq data and upregulated genes in TCGA tumor samples and defined genes identified in all three analyses as CAFs-related genes (CRGs). We extracted a CRG signature using Least Absolute Shrinkage and Selection Operator analysis and investigated its biological mechanisms by combining Gene Set Enrichment Analysis and the AUCell algorithm. The Tumor Immune Dysfunction and Exclusion algorithm and the IMvigor 210 dataset were employed to assess the signature's capability to predict immunotherapeutic responses. Additionally, we analyzed the relationship between the signature and the IC 50 of targeted agents. In vitro validation confirmed the relative mRNA expression of the CRGs and the function of CERCAM., Results: The CRG signature was anchored on six genes: CERCAM, TMEM132A, TIMP1, P4HA3, FKBP10, and CEBPB. Kaplan-Meier analysis indicated that patients with high expression of the signature experienced poorer survival than those with low expression. Furthermore, immunotherapy was more effective in patients with low signature expression. In vitro assays revealed CERCAM silencing led to a substantial reduction in the proliferative and migratory capacities of ccRCC cell lines., Conclusion: Our CRG signature holds promise in forecasting prognosis and guiding personalized treatment for patients with ccRCC., Competing Interests: None., (AJTR Copyright © 2024.)